A-LevelBiologyImmunity9700/22 · May/June 2017 · Q511 Marks

Some pathogens can enter the human body through the gas exchange system.

(a)(i)The epithelial lining of the gas exchange system is adapted for defence against pathogens. List the structures in the gas exchange system that have a ciliated epithelial lining.[1]
(a)(ii)Name the cells in the ciliated epithelium that synthesise and secrete mucus.[1]
(b)Alveolar macrophages are cells of the immune system. They have an important role in defence against respiratory infections. The infectious lung disease, pneumonia, can be caused by Streptococcus pneumoniae. Most healthy people inhaling air containing these bacteria do not become ill because of the action of the alveolar macrophages. Outline the mode of action of an alveolar macrophage in response to the presence of S. pneumoniae. You may use diagrams with notes to help your answer.[3]
(c)Irritants in tobacco smoke can contribute to emphysema, one of the chronic obstructive pulmonary disorders (COPD). In emphysema, the alveoli lose their ability to recoil on expiration and can burst. Suggest how the structure of the alveolar wall changes so that an alveolus bursts.[2]
(d)Some alveolar cells produce a surfactant that helps to prevent the collapse of alveoli on exhalation. Too much surfactant decreases the efficiency of gas exchange in the alveoli. A glycoprotein known as GM-CSF is released by some cells of the immune system when there is too much surfactant in the alveoli. Excess surfactant is then broken down by alveolar macrophages. Receptors for GM-CSF are on the cell surface membranes of alveolar macrophages. Explain how maintaining the correct quantity of surfactant in the alveoli is the result of a cell signalling mechanism.[4]

Mark scheme

Marking points from the official mark scheme (May/June 2017). The mark or mark type is shown in brackets.

[1] trachea / windpipe + bronchus / bronchi + bronchiole / bronchioles ; treat as neutral type of bronchiole
[1] goblet ;
[1] recognition / AW / binding / attachment, (of macrophage) to, bacterium / S. pneumoniae /(bacterial) antigen ; A detects / identifies (D) must label, bacteria/S. pneumoniae, or macrophage and show bacterium attached
[1] endocytosis / phagocytosis ;
[1] described; e.g. engulfing / enveloping / pseudopodia surround phagocytic / endocytotic, vacuole formed A phagosome A vesicle
[1] fusion of lysosome(s) (to vacuole) ; (D) must label lysosome
[1] breakdown / destruction / digestion / AW, of bacterium / S. pneumoniae ; A kills (D) annotated on diagram
[1] ref. to, hydrolytic / digestive, enzymes ; A named digestive enzymes must be in context of lysosome (D) labelled as such
[1] elastin broken down / elastic fibres damaged ; A elastic fibres broken down A less, elastin / elastic fibres
[1] (alveolar) wall becomes overstretched / AW weakened (alveolar) wall / AW e.g. cannot withstand higher pressure bursts on inhalation (bronchioles collapse) on exhalation, trapped / remaining, air bursts alveoli
[1] (excess surfactant) stimulates immune system cells ;
[1] release/ secretion, of, GM-CSF ; I produce
[1] GM-CSF is a signal or GM-CSF is a signalling, molecule / protein / glycoprotein; A messaging molecule
[1] binds to / combines with / AW, (cell surface membrane) receptors (on alveolar macrophages);
[1] ref. to specificity ; A described as GM-CSF receptor complementary shape for GM-CSF
[1] leads to / sets off / triggers / AW, response (in the cell) / removal of surfactant; in context of macrophage A stimulates
[1] detail; e.g. triggers secondary messenger activates enzymes / enzyme cascade signal transduction phosphorylation events